This proposal focuses on the locus, characteristics, mechanisms and cardiovascular significance of interactions between one sympathoinhibitory system, the dorsolateral spinal sympathoinhibitory system (DSSS), and other sympathomodulatory systems. We will explicitly test the role of these interactions in the regulation of sympathetic activity and arterial blood pressure. The DSSS has been assumed to be a descending pathway. We will determine whether have been antidromically stimulated in previous studies. DSSS inhibition can be abolished or "gated" at a spinal level by a pathway which descends from the caudal medulla. Thus, even if the DSSS exists only at spinal levels and inhibits only spinal sympathetic generators, its action can be coordinated with supraspinal mechanisms. We will determine the medullary origin and spinal course of this pathway. We will compare the properties of the "gating" system in hypertensive and normotensive rats, for we suspect that the DSSS may be defective in spontaneously hypertensive rats. We will compare spinal interactions between the DSSS and a variety of sources of sympathetic excitation. Preliminary data suggest the DSSS is highly specific for spontaneous sympathetic activity and sympathetic after-discharges. We will study these interactions in spontaneously hypertensive and normotensive rats because we suspect that deficits in some interactions may result in sympathetic hyperactivity. We will use single-unit recording techniques to identify spinal interneurons which play a role in interactions between the DSSS and excitatory systems. The convergence of inputs (afferent and descending excitatory, DSSS inhibitory, and "gating") will permit us to identify the relative positions of classes if interneurons in intraspinal sympathetic networks. Finally, we will test the hypothesis that the same interneurons mediate both DSSS inhibition and postexcitatory sympathoinhibition (the "sympathetic silent period").